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Stimulation of the intracerebral noadrenergic pathway (INP) increases hypothalamic blood flow as measured in conscious rabbits using a 133xenon washout technique. This increase is abolished by the intra-hypothalamic injection of 0.65 micrograms of the muscarinic antagonist atropine and by 5 micrograms of the nicotinic antagonist mecamylamine. Further, 1 micrograms of the cholinomimetic methacholine produces a similar vasodilation. While methacholine enhances the vasodilatation on stimulation of the INP, destruction of the pathway abolishes the entire vasodilator response to methacloline. Removal of the superior cervical sympathetic ganglia does not abolish vasodilatation. A role for endogenous acetylcholine in the INP-induced vasodilatation is thus proposed. This vasodilatation appears to act via an increase in neuronal activity with a resultant lowering of local pH, as 60 micrograms barbiturate and intra-hypothalamic bicarbonate abolish the dilatation completely. The cholinergic vasodilatation reported here is probably an excitatory effect on the INP and is not likely to be due to an inhibition of sympathetic vasoconstrictor tone.
Klugman et al. (Mon,) studied this question.